269
tion. It is important that the extent of this problem should be determined, particularly
because the use of A-protein as an antigenic component of a potential vaccine for
control of diseases caused by Aer. salmonicida has been advocated. This is due to
the apparent immunological relatedness of the A-protein among isolates from different locations and a variety of fi sh hosts (Evenberg et al. 1982 ). In view of the
existence of virulent, auto-agglutinating Aer. salmonicida strains apparently lacking
the A-layer, the effectiveness of such a vaccine would possibly be subject to severe
limitations.
Type I Pilus System
Using knockout mutants, it was concluded that the type I pilus system was not
important for invasion but was for subsequent colonization (Dacanay et al. 2010 ).
Type III Secretion System
A type III secretion system, which utilises a 140 kbp pAsa5 plasmid and
chromosome- encoded transmembrane injection devise incorporating membrane
proteins and a needle-like structure to translocate the effector protein AexT toxin
from the cytosol into the host cell, has been linked to the virulence of Aer. salmonicida subsp. salmonicida and in particular the ability to achieve a systemic infection
(Burr et al. 2002 , 2003a , b , 2005 ; Stuber et al. 2003 ; Dacanay et al. 2006 ; Ebanks
et al. 2006 ; Tanaka et al. 2012 ). In the case of one culture A449, the expression of
the type III secretion system was temperature dependent, being active within 30 min
at 28 °C especially followed by exposure to low levels of calcium but not 17 °C,
which is more usual for the outbreak of disease (Ebanks et al. 2006 ). However,
expression was induced at 16 °C in the presence of 0.19 to 0.38 M NaCl. A second
effector protein, AopP, has been identifi ed, and found to inhibit the NF-kB pathway
downstream of 1kB kinase activation. The gene was found to encoded on a small
~6.4 kb plasmid (Fehr et al. 2006 ). The effector genes, aexT; this codes for ADP
(ribosyltransferase; Burr et al. 2003a , b ) , oapH and aopO, and ascC, which is the
gene encoding the outer membrane pore of the secretion system, were inactivated
by deletion and the effects examined in Atlantic salmon. The outcome was that the
∆ ascC mutant was not virulent. However, i.p. injection of ∆ aexT, ∆ aopH and ∆
aopO resulted in disease, which was regarded as being indistinguishable from the
parental wild-type culture. The conclusion was that whereas the type III secretion
system was essential for virulence, the individual effectors were less signifi cant for
virulence but were for colonisation (Dacanay et al. 2006 ).
Aeromonas salmonicida
tion. It is important that the extent of this problem should be determined, particularly
because the use of A-protein as an antigenic component of a potential vaccine for
control of diseases caused by Aer. salmonicida has been advocated. This is due to
the apparent immunological relatedness of the A-protein among isolates from different locations and a variety of fi sh hosts (Evenberg et al. 1982 ). In view of the
existence of virulent, auto-agglutinating Aer. salmonicida strains apparently lacking
the A-layer, the effectiveness of such a vaccine would possibly be subject to severe
limitations.
Type I Pilus System
Using knockout mutants, it was concluded that the type I pilus system was not
important for invasion but was for subsequent colonization (Dacanay et al. 2010 ).
Type III Secretion System
A type III secretion system, which utilises a 140 kbp pAsa5 plasmid and
chromosome- encoded transmembrane injection devise incorporating membrane
proteins and a needle-like structure to translocate the effector protein AexT toxin
from the cytosol into the host cell, has been linked to the virulence of Aer. salmonicida subsp. salmonicida and in particular the ability to achieve a systemic infection
(Burr et al. 2002 , 2003a , b , 2005 ; Stuber et al. 2003 ; Dacanay et al. 2006 ; Ebanks
et al. 2006 ; Tanaka et al. 2012 ). In the case of one culture A449, the expression of
the type III secretion system was temperature dependent, being active within 30 min
at 28 °C especially followed by exposure to low levels of calcium but not 17 °C,
which is more usual for the outbreak of disease (Ebanks et al. 2006 ). However,
expression was induced at 16 °C in the presence of 0.19 to 0.38 M NaCl. A second
effector protein, AopP, has been identifi ed, and found to inhibit the NF-kB pathway
downstream of 1kB kinase activation. The gene was found to encoded on a small
~6.4 kb plasmid (Fehr et al. 2006 ). The effector genes, aexT; this codes for ADP
(ribosyltransferase; Burr et al. 2003a , b ) , oapH and aopO, and ascC, which is the
gene encoding the outer membrane pore of the secretion system, were inactivated
by deletion and the effects examined in Atlantic salmon. The outcome was that the
∆ ascC mutant was not virulent. However, i.p. injection of ∆ aexT, ∆ aopH and ∆
aopO resulted in disease, which was regarded as being indistinguishable from the
parental wild-type culture. The conclusion was that whereas the type III secretion
system was essential for virulence, the individual effectors were less signifi cant for
virulence but were for colonisation (Dacanay et al. 2006 ).
Aeromonas salmonicida